Gastric Biopsy in the Megaloblastic Anaemias

Wm, Davidson; Jl, Markson

doi:10.1177/003693305600100803

Cited by 13 publications

(10 citation statements)

References 24 publications

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“…Some authors have reported residual parietal cells in up to 32% of their cases 0-_ (Williams et al, 1958), and similar findings were noted by Markson and Davidson (1956), and Shiner and Doniach (1957). Whether these cells are functional or not is unclear, but they persist in the face of histamine-fast achlorhydria.…”

Section: Discussionmentioning

confidence: 57%

Gastric morphology and serum gastrin levels in pernicious anaemia.

Lewin¹,

Dowling²,

Wright³

et al. 1976

Gut

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SUMMARY Mucosal biopsies from multiple sites in the stomachs of 21 patients with pernicious anaemia have been examined. The histological changes almost always involved the entire gastric mucosa, including that of the pyloric antrum. Metaplastic changes were almost universal and consisted of intestinal metaplasia in the body and antrum and pyloric metaplasia in the body. The severity of the pyloric metaplasia was such as to make the distinction between body and antrum on biopsy impossible. No relationship was found between serum gastrin activity and the histological appearances of the gastric antrum or body.The past 25 years have witnessed the introduction of techniques whose application has contributed substantially to the investigation of the nature of chronic gastritis. Peroral suction biopsy (Wood et al., 1949;Joske et al., 1955) of the body and fundus of the stomach has provided a solid histological foundation which, in conjunction with measurements of gastric secretion of acid (Bock et al., 1963) and intrinsic factor and the detection of gastric antibodies (te Velde et al., 1966;Fisher et al., 1967), has considerably extended our knowledge of the pathophysiology of the body of the stomach.In contrast, the structure and function of the gastric antrum was until recently little studied. The introduction of the fibreoptic gastroscope made possible multiple biopsying of the gastric mucosa from well-defined sites in the body and pyloric antrum (Seifert and Knoll, 1968;Konturek and Urban, 1969; Ottenjann et al., 1969a, b) Methods PATIENTSEighteen patients (14 women and four men) referred to our clinic at Stanford University Medical Center with established or suspected PA were studied. Diagnosis was established by failure to secrete detectable acid in response to a maximal dose of gastric stimulant (betazole 1-7 mg/kg body weight) and urinary excretion of less than 10% of a 0-5 Kg oral dose of 57Co B12 in a standard Schilling test, which was corrected with added gastric intrinsic factor. Supporting evidence was low serum vitamin B12 activity, low or absent gastric intrinsic factor secretion, and the presence of circulating gastric antibodies.In addition, studies are included of three patients who were referred for suspected PA but in whom the above criteria were not completely fulfilled (Table 1).

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Section: Discussionmentioning

confidence: 57%

Gastric morphology and serum gastrin levels in pernicious anaemia.

Lewin¹,

Dowling²,

Wright³

et al. 1976

Gut

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“…Second, at the present time, it is not possible to make a definitive diagnosis of achlorhydria in an individual patient due to lack of histamine or pentagastrin to stimulate gastric acid secretion. Because almost all patients with achlorhydria associated with PA have atrophic gastritis or gastric atrophy (97), gastric biopsy might logically be considered a surrogate for gastric analysis in diagnosing achlorhydria. However, 25-30% of patients with achlorhydria not associated with PA do not have gastric atrophy (19,97).…”

Section: Discussionmentioning

confidence: 99%

“…Because almost all patients with achlorhydria associated with PA have atrophic gastritis or gastric atrophy (97), gastric biopsy might logically be considered a surrogate for gastric analysis in diagnosing achlorhydria. However, 25-30% of patients with achlorhydria not associated with PA do not have gastric atrophy (19,97). Moreover, in 23% of control subjects, gastric biopsy samples showed atrophic gastritis or gastric atrophy (97).…”

Section: Discussionmentioning

confidence: 99%

“…However, 25-30% of patients with achlorhydria not associated with PA do not have gastric atrophy (19,97). Moreover, in 23% of control subjects, gastric biopsy samples showed atrophic gastritis or gastric atrophy (97). Therefore, gastric biopsy alone is not a reliable indicator of the presence or absence of achlorhydria in an individual patient.…”

Section: Discussionmentioning

confidence: 99%

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Is achlorhydria a cause of iron deficiency anemia?

Betesh

Ana

Cole

et al. 2015

The American Journal of Clinical Nutrition

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We re-evaluated the old hypothesis that gastritis-induced achlorhydria is a cause of iron deficiency anemia (IDA) in humans. First, we analyzed the currently available research on the association between achlorhydria and IDA. When gastric acid secretion was measured after maximal stimulation, the frequency of achlorhydria (or severe hypochlorhydria) was 44% in patients with idiopathic IDA and 1.8% in healthy controls. In some patients with pernicious anemia, presumed achlorhydria preceded the development of IDA in time. However, we found no credible evidence that IDA caused gastritis or that IDA preceded the development of achlorhydria. Thus, correlational results favor achlorhydria as the causal factor in the association between achlorhydria and IDA. Second, we sought to determine whether gastritis and achlorhydria cause negative iron balance. When biosynthetic methods were used to isotopically label iron in food, achlorhydric patients were found to have severe malabsorption of nonheme iron, which persisted after the development of IDA. In 1 study, achlorhydria reduced the normal increase in heme-iron absorption from hemoglobin in response to iron deficiency. After an injection of isotopic iron into normal men, the physiologic loss of iron from the body was found to be 1 mg/d. Patients with chronic gastritis had excess fecal loss of isotopically tagged plasma iron. Calculations based on these results indicate that the absorption of iron from a typical Western diet by achlorhydric patients would be less than physiologic iron losses, creating a negative iron balance that could not be overcome by the adaptive increase in duodenal iron absorptive capacity that occurs in response to iron deficiency. The combination of results from these correlational and pathophysiologic studies supports the hypothesis that gastritis-induced achlorhydria can be an independent cause of IDA.

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“…The natural course of Hashimoto's disease would appear to be a progression from a diffuse thyroiditis in which round-cell infiltration predominates to a state in which fibrosis and loss of acini are the most notable features. Markson and Davidson (1956) have suggested that the gastric atrophy commonly found in pernicious anaemia may be an endresult of severe atrophic gastritis. Thus the pathological processes in these two diseases may be of similar type.…”

Section: Discussioinmentioning

confidence: 99%